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DNA Repair (Amst). 2019 May;77:87-95. doi: 10.1016/j.dnarep.2019.03.007. Epub 2019 Mar 15.

SWI/SNF: Complex complexes in genome stability and cancer.

Author information

1
Department of Molecular Genetics, Oncode Institute, Erasmus MC, University Medical Center Rotterdam, Dr. Molewaterplein 40, 3015 GD, Rotterdam, the Netherlands.
2
Department of Molecular Genetics, Oncode Institute, Erasmus MC, University Medical Center Rotterdam, Dr. Molewaterplein 40, 3015 GD, Rotterdam, the Netherlands. Electronic address: w.vermeulen@erasmusmc.nl.
3
Department of Molecular Genetics, Oncode Institute, Erasmus MC, University Medical Center Rotterdam, Dr. Molewaterplein 40, 3015 GD, Rotterdam, the Netherlands. Electronic address: w.lans@erasmusmc.nl.

Abstract

SWI/SNF complexes are among the most studied ATP-dependent chromatin remodeling complexes, mostly due to their critical role in coordinating chromatin architecture and gene expression. Mutations in genes encoding SWI/SNF subunits are frequently observed in a large variety of human cancers, suggesting that one or more of the multiple SWI/SNF functions protect against tumorigenesis. Chromatin remodeling is an integral component of the DNA damage response (DDR), which safeguards against DNA damage-induced genome instability and tumorigenesis by removing DNA damage through interconnected DNA repair and signaling pathways. SWI/SNF has been implicated in facilitating repair of double-strand breaks, by non-homologous end-joining as well as homologous recombination, and repair of helix-distorting DNA damage by nucleotide excision repair. Here, we review current knowledge on SWI/SNF activity in the DDR and discuss the potential of exploiting DDR-related vulnerabilities due to SWI/SNF dysfunction for precision cancer therapy.

KEYWORDS:

Cancer therapy; DNA damage response; Homologous recombination; Non-homologous end-joining; Nucleotide excision repair; SWI/SNF

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